Amon U, von Stebut E, von Gizycki U, Wolff H H
Department of Dermatology, Medical University of Lübeck, Germany.
Agents Actions. 1994 Jun;41 Spec No:C9-10. doi: 10.1007/BF02007744.
Arachidonic acid metabolites generated from activated basophils and/or mast cells mediate different types of cutaneous inflammatory reactions. To clarify the mechanisms of leukotriene C4 (LTC4) production from human basophils, cells were purified from the peripheral blood by negative selection with immunobeads. The protein kinase C (PKC) activators 12-O-tetradecanoyl-phorbol-13-acetate, phorbol-12,13-dibutyrate and phorbol-12,13-didecanoate did not induce a significant LTC4 generation from human basophils in vitro, indicating that phorbol-ester-sensitive PKC isozymes are not involved in the mechanisms of arachidonic acid metabolism in these cells. However, selective PKC inhibitors (Ro 31-7549, ilmofosine, GF109203X, and calphostin C) potentiated the IgE-mediated LTC4 production in a dose-dependent fashion. We therefore suggest that PKC isozymes which are influenced by these inhibitors modulate the degree of LTC4 release after stimulation with anti-IgE antibodies.
由活化的嗜碱性粒细胞和/或肥大细胞产生的花生四烯酸代谢产物介导不同类型的皮肤炎症反应。为阐明人嗜碱性粒细胞产生白三烯C4（LTC4）的机制，通过免疫磁珠阴性选择从外周血中纯化细胞。蛋白激酶C（PKC）激活剂12-O-十四烷酰佛波醇-13-乙酸酯、佛波醇-12,13-二丁酸酯和佛波醇-12,13-二癸酸酯在体外未诱导人嗜碱性粒细胞产生显著的LTC4，表明佛波酯敏感的PKC同工酶不参与这些细胞中花生四烯酸代谢机制。然而，选择性PKC抑制剂（Ro 31-7549、 ilmofosine、GF109203X和钙泊三醇）以剂量依赖方式增强了IgE介导的LTC4产生。因此，我们认为受这些抑制剂影响的PKC同工酶在抗IgE抗体刺激后调节LTC4释放程度。
